Abstract

Strongyloides (S.) stercoralis and Human T-Lymphotropic Virus 1 (HTLV-1) share some endemic regions such as Japan, Jamaica, and South America and are mostly diagnosed elsewhere in immigrants from endemic areas. This co-infection has not been documented in Argentina although both pathogens are endemic in the Northwest. We present a case of S. stercoralis and HTLV-1 co-infection with an initial presentation due to gastrointestinal symptoms which presented neither eosinophilia nor the presence of larvae in stool samples in a non-endemic area for these infections. A young Peruvian woman living in Buenos Aires attended several emergency rooms and finally ended up admitted in a gastroenterology ward due to incoercible vomiting, diarrhea, abdominal pain, fever, and weight loss. Gastrointestinal symptoms started 3 months before she returned to Argentina from a trip to Peru. She presented malnutrition and abdominal distension parameters. HIV-1 and other immunodeficiencies were discarded. The serial coproparasitological test was negative. Computed tomography showed diffuse thickening of duodenal and jejunal walls. At the beginning, vasculitis was suspected and corticosteroid therapy was initiated. The patient worsened rapidly. Skin, new enteral biopsies, and a new set of coproparasitological samples revealed S. stercoralis. Then, HTLV-1 was suspected and infection was confirmed. Ivermectin and albendazole were administrated, until the stool sample remained negative for 2 weeks. Larvae were not observed in fresh stool, Ritchie method, and agar culture 1 week post-treatment. Although she required initial support with parenteral nutrition due to oral intolerance she slowly progressed favorably. It has been highly recommended to include a rapid and sensitive PCR strategy in the algorithm to confirm Strongyloides infection, which has demonstrated to improve early diagnosis in patients at-risk of disseminated strongyloidiasis.

Highlights

  • The soil-transmitted nematode Strongyloides stercoralis (S.) is estimated to infect at least 30–100 million people

  • The high production of IFN-γ observed in co-infected patients induced by a Th1 profile results in a failure of activation of eosinophils and reduction of their numbers

  • This decreases the defense mechanisms against helminthes leading to an increased risk of severe forms of strongyloidiasis without eosinophilia (Porto et al, 2001) In this context, it has been hypothesized that dissemination of Strongyloides infection could occur due to an increase in the number of regulatory T cell (Montes et al, 2009)

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Summary

INTRODUCTION

The soil-transmitted nematode Strongyloides stercoralis (S.) is estimated to infect at least 30–100 million people. When auto-infection occurs, the development of disseminated strongyloidiasis is possible, especially in immunocompromised hosts like patients treated with corticosteroids, cancer patients and persons infected with human T-lymphotropic virus (HTLV-1) (Ramanathan and Nutman, 2008). In these cases, hyperinfection, characterized by gastrointestinal and pulmonary hemorrhage, and secondary bacterial infections can occur (Keiser and Nutman, 2004). HTLV-1 infected carriers seem to have an increased risk of acquiring strongyloidiasis indicating a possible subclinical immunodeficiency This retrovirus predisposes patients to recurrent and severe infection with S. stercoralis (Carvalho and Da Fonseca Porto, 2004). For hyperinfection syndrome and disseminated infections, ivermectin is the drug of choice with albendazole as a secondline therapy, until complete eradication of the parasite is achieved (Gann et al, 1994; Mejia and Nutman, 2012)

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